NOTA-cRY9M
NOTA-cRY9M is a reagent targeting FGFR1 with a Kd value of 58 nM, and exhibits subtype selectivity for FGFR2-4. When radiolabeled as [68Ga]Ga-NOTA-cRY9M, it functions as a stabilizer, imaging contrast enhancer, and tumor-targeting agent, and accumulates in FGFR1-positive non-small cell lung cancer xenograft models. NOTA-cRY9M can be used in studies related to non-small cell lung cancer.
For research use only. We do not sell to patients.
- Formula: C71H108N26O17
- Molecular Weight:1597.78
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
FGFR1 58 nM (Kd) |
In Vitro
68Ga]Ga-NOTA-cRY9M (74 kBq per well; 15-120 min) exhibits time-dependent, FGFR1-specific cellular uptake in Calu-3 and NCI-H520 NSCLC cells, with significantly lower uptake in FGFR1-negative NCI-H2170 cells[1].
[68Ga]Ga-NOTA-cRY9M (74 kBq per well; 10-11-10-2 M unlabeled peptide; 2 h) exhibits high FGFR1-binding affinity in Calu-3 cells, with an IC50 of 62 nM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nude (male, 4-5 weeks old, 18-21 g)[1]
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Dosage:3.7 MBq
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Administration:i.v.; single dose
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Result:Achieved peak tumor uptake of 3.69 %ID/g at 10 minutes postinjection, with uptake declining gradually to 3.33 %ID/g by 60 minutes.
Reached a maximum tumor-to-muscle ratio of 5.56 at 60 minutes, with tumor-to-liver and tumor-to-lung ratios reaching approximately 2.3 and 3.3, respectively, at 60 minutes.
Exhibited primarily renal excretion with low hepatic retention.\nAchieved peak tumor uptake of 3.11 %ID/g at 10 minutes postinjection.
Reached a maximum tumor-to-muscle ratio of 4.10 at 60 minutes.
Showed tumor uptake of 2.61 %ID/g in ex vivo biodistribution at 60 minutes.\nAchieved a maximum tumor uptake of 1.20 %ID/g, with a consistently low tumor-to-muscle ratio of 1.42 throughout the 60-minute imaging window.
Showed tumor uptake of 0.91 %ID/g in ex vivo biodistribution at 60 minutes.\nShowed a substantial reduction in [68Ga]Ga-NOTA-cRY9M uptake (1.10 %ID/g) in FGFR1-knockdown Calu-3 xenografts compared to control Calu-3 tumors (3.83 %ID/g), with a corresponding tumor-to-muscle ratio of 2.11 vs. 5.89 in controls.
Chemical Information
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Molecular Weight 1597.78
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Formula C71H108N26O17
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Sequence
Cyclo(Arg-Trp-Arg-{Lys(NOTA)}-Gln-Thr-Arg-His-Tyr)
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Sequence Shortening
Cyclo(RWR-{Lys(NOTA)}-QTRHY)
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Patient-Derived Xenograft (PDX)
Patient-derived xenograft (PDX) models are generated by engrafting primary human tumor tissue directly into immunodeficient mice, allowing in vivo propagation of patient tumor biology without initial in vitro adaptation. These models are used to preserve key histopathological and molecular characteristics of the original tumor and enable assessment of tumor growth dynamics and therapeutic response in a living organism. The biological readout is tumor engraftment and subsequent growth in the murine host, which reflects the ability of human tumor cells to survive, vascularize, and expand in an immunocompromised microenvironment.
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Splenic/Portal-Vein Liver Metastasis Xenograft
Splenic and portal-vein liver metastasis xenograft models deliver tumor cells into the portal circulation so that cells reach the liver first and form hepatic metastatic lesions; splenic injection uses the spleen as an access route to the portal system, while direct portal-vein injection introduces cells into the portal vein without requiring splenectomy. The assay detects liver colonization, intrahepatic tumor growth, tumor distribution, treatment response, survival, and liver-metastasis microenvironment changes; readouts include bioluminescence or fluorescence imaging, gross liver nodule counts, liver weight or tumor burden, histology, and survival.
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Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
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Orthotopic Cell-Line Xenograft
Orthotopic cell-line xenograft models involve implantation of human cancer cell lines into the anatomically corresponding organ of immunodeficient mice to reproduce tumor growth within a native microenvironment, enabling more clinically relevant tumor behavior compared with subcutaneous models. These models are widely used because orthotopic placement better recapitulates tumor progression, including invasion and metastatic spread, which are often underrepresented in heterotopic implantation systems. Compared with conventional xenografts, orthotopic implantation is described as more technically complex but provides improved simulation of tumor-microenvironment interactions and metastatic behavior, making it particularly valuable for translational oncology research. Surgical orthotopic implantation approaches have been emphasized as enabling faithful reproduction of clinical cancer features, including metastasis and disease progression patterns that align with the tumor’s organ of origi
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Intraperitoneal/Peritoneal Dissemination Xenograft
Intraperitoneal (IP) or peritoneal dissemination xenograft models are based on the introduction of human cancer cells into the peritoneal cavity of immunodeficient mice, where they attach to peritoneal surfaces, form multicellular aggregates or spheroids, and progressively generate disseminated tumor nodules that mimic advanced peritoneal metastatic disease. These models are widely used to study ovarian cancer progression, tumor-microenvironment interactions, and intraperitoneal therapeutic responses, often incorporating bioluminescence or fluorescence imaging to longitudinally monitor tumor burden in vivo. The biological principle relies on the capacity of tumor cells such as SKOV3 or related ovarian carcinoma lines to survive in suspension, aggregate within ascites-like fluid, adhere to mesothelial surfaces, and invade peritoneal organs, thereby recapitulating human peritoneal carcinomatosis patterns observed in advanced disease.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)